Our objective is to identify specific genetic loci controlling blood pressure in the salt sensitive (S) and salt resistant (R) rats of Dahl. Considerable effort has been made to develop criteria by which one can establish cause and effect relationships between a genetic marker and blood pressure. This is done by looking at biochemical/physiological systems which may influence blood pressure in order to find traits that show a marked contrast between the S and R strains. Such traits are studied genetically to determine the mode of inheritance (one or several loci, type of Mendelian inheritance for single loci). Traits are then studied in genetically segregating populations (F2 and backcross populations produced from an SxR cross) in order to determine if a specific trait and an increment in blood pressure segregate together. Specific traits under consideration are urinary kallikrein and (Na plus K ions)-activated ATPase. Another goal is to examine the role that mineralocorticoid induced changes may play in determining blood pressure in S and R rats. A method is devised to use the relationship between skeletal muscle K ion and blood pressure in order to dissect genetically induced blood pressure changes into two components, one related to mineralocorticoid-like activity, and another not related to mineralocorticoid-like activity. The utility of such a quantitative division would be to focus work in one area or the other. A final specific objective is to try to relate the marked accumulation of albumin fragments, seen in the pituitaries of R rats, to pituitary proteinase enzymes. Experiments on cross transplantation of pituitaries between S and R rats will also be undertaken to try to determine if the striking accumulation of albumin fragments in the pituitary of R rats has a biological meaning with regard to blood pressure.